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首页> 外文期刊>Journal of Pathology: Journal of the Pathological Society of Great Britain and Ireland >Regulation of cathepsin X overexpression in H. pylori-infected gastric epithelial cells and macrophages.
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Regulation of cathepsin X overexpression in H. pylori-infected gastric epithelial cells and macrophages.

机译：组织蛋白酶X在幽门螺杆菌感染的胃上皮细胞和巨噬细胞中过表达的调节。

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Cathepsin X (CTSX) is strongly up-regulated in Helicobacter pylori-infected gastric mucosa and intestinal-type gastric cancer. The overexpression of CTSX is mediated predominantly by associated macrophages; depends on a functional type IV-secretion system; and leads to increased migration of gastric epithelial cells. In the present study, we analysed the role of CagA in CTSX overexpression and identified H. pylori-induced inflammatory factors and signalling pathways required for stimulating CTSX expression by H. pylori. Gastric epithelial cells were co-cultured with macrophages in Transwell chambers of 0.4 microm pore size, enabling exchange of fluids but retracting H. pylori. N87 gastric epithelial cells were infected with H. pylori P1 wild-type strain in the presence of inhibitors for p38, JNK, and ERK1/2 signal transduction pathways. Furthermore, cytokines and growth factors were tested for their regulatory function using inhibitory antibodies, and their gene expression was studied by quantitative RT-PCRs and western blots. CTSX is strongly up-regulated at both the mRNA and the protein levels by TNF-alpha, IL-1beta, IL-6, and IL-8, depending on cell type. All these cytokines were found to be increased by five- to ten-fold in macrophages by H. pylori infection of co-cultured N87 gastric epithelial cells. In macrophages, H. pylori up-regulated CTSX via ERK1/2 signalling pathways, and in N87 cells via JNK irrespective of p38 signalling. Our results suggest that H. pylori induced overexpression of CTSX in macrophages and epithelium through specific cytokines that are initiated by CagA-dependent pathways in a cell type-dependent manner.
机译：组织蛋白酶X（CTSX）在幽门螺杆菌感染的胃粘膜和肠型胃癌中被上调。 CTSX的过表达主要由相关的巨噬细胞介导。取决于功能性IV分泌系统;并导致胃上皮细胞迁移增加。在本研究中，我们分析了CagA在CTSX过表达中的作用，并确定了幽门螺杆菌诱导的炎症因子和通过幽门螺杆菌刺激CTSX表达所需的信号通路。胃上皮细胞与巨噬细胞在0.4微米孔径的Transwell腔室中共培养，从而能够交换液体但使幽门螺杆菌收缩。在p38，JNK和ERK1 / 2信号转导抑制剂存在的情况下，用幽门螺杆菌P1野生型菌株感染N87胃上皮细胞。此外，使用抑制性抗体测试了细胞因子和生长因子的调节功能，并通过定量RT-PCR和Western印迹研究了它们的基因表达。取决于细胞类型，TNF-α，IL-1β，IL-6和IL-8会在mRNA和蛋白质水平上强烈上调CTSX。发现通过共培养的N87胃上皮细胞的幽门螺杆菌感染，所有这些细胞因子在巨噬细胞中增加了五至十倍。在巨噬细胞中，幽门螺杆菌通过ERK1 / 2信号通路上调CTSX，在N87细胞中通过JNK上调，而与p38信号无关。我们的研究结果表明幽门螺杆菌通过特定的细胞因子诱导巨噬细胞和上皮细胞中CTSX的过度表达，这些细胞因子是由CagA依赖性途径以细胞类型依赖性方式启动的。

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